TheTruthAboutStuff.com
Review 2 - Published December 2007
Monte WC. 2007, A Deadly Experiment – (Fitness Life 2007 Dec.34:38-42)
We cannot introduce a poison into the food supply without paying a terrible price, and I am convinced that this tragic scenario has and is playing itself out. In an earlier article regarding the dangers of Aspartame (Fitness Life 2007 Nov 33:31-33), I explained how this artificial sweetener can degrade into methanol and then into formaldehyde, and I touched on some of the deleterious effects of formaldehyde on the human body. In this article I make the case that increased methanol consumption is implicated in the appearance and increased incidence of multiple sclerosis (MS) and that Aspartame consumption is one of the two primary sources of methanol in our diets.
What Price Aspartame: The Early Warnings Ignored
We have consumption data for Aspartame in the United States from mid-1981 when a ban on its use was reversed through political intervention (39). The increase in production and consumption was relatively slow until a surge occurred when approval came for its use in carbonated beverages. Although we would wish such periods did not occur, a period in which a substance is introduced into the diet of an unsuspecting population is a perfect time to look for anomalies that can help us to hypothesize about the extent to which the substance may be toxic. I examined data on diseases and conditions that I thought might be affected by the increased consumption of Aspartame such as depression, autoimmunity, and birth defects (terata). Both methanol and Aspartame are proven teratogens in animals far less sensitive to methanol than humans (92,96,103-105,124,159,177). Data from the US National Center for Health Statistics regarding morbidity numbers during those critical early years are presented here in graphic form.
These are the original data with no modification save for those regarding autism; these were displaced by six years because the data presented to me were for patients diagnosed at six years of age(98). This displacement reflects that exposure to methanol occurred in the womb.
If these data teach us anything they teach us that the first question we should ask a depressed child is “Do you drink diet soda?”…and that pregnancy is not the time to consume Aspartame(100).
It is interesting to note that Breast Cancer has the same worldwide distribution and incidence characteristics as MS (190) and shares with MS the known, methanol rich, causal agentÂ…cigarette smoking.
I found the most striking graph to be the one showing increase in diagnosed cases of multiple sclerosis. It usually takes, at least, 10 years from first onset of symptoms to reportable diagnosis of the disease(86,167). This early reporting was evidence, to me, of much worse to follow.
Science has been seeking the cause of multiple sclerosis for 150 years. It has repeatedly been suggested there is evidence to implicate a small toxic molecule(153,185)Â… a solvent(74,140). Methanol is the smallest of solvents.
The results of 27 years of Aspartame consumption
The Worst of Timing
The 1980’s was well into the era when laboratories that had been performing methanol toxicity research were being paid by the company who invented Aspartame to prove the safety of its sweetener(121,131). Dr. Hugo Henzi, an M.D. now deceased, published a book in 1980 purporting to prove dietary methanol as the cause of multiple sclerosis(5). His clinical logic and anatomical observations were impeccable (6,8-10), but he made a major mistake. He erroneously believed that the methanol that caused MS came from “fresh” fruits and vegetables, and as a consequence, he proposed a curative diet that we now know had little chance of success(101). However, several lines of evidence are now converging to support Dr. Henzi’s primary assertion.
The Secret Battle that is Autoimmunity
From an early moment in the evolution of manÂ…from as far back as the mutation that accounted for universality in its distributionÂ… a biochemical battle has quietly raged within the most intimate anatomy of the human body. Two alcohols competing for the attention of a serendipitously distributed and poorly understood enzymeÂ… an enzyme that, by accident, has become the lonely suitor to and only benefactor of their advances. The outcome, after years of struggle, determines who will and who will not die with MS.
The alcohols are ethyl and methyl alcohol. Methanol is the smallest known alcohol containing only one carbon atom; ethanol has two carbon atoms. The enzyme has had several names as it has been discovered and rediscovered over the years in the physiological, neurological, and opthomological sciences. However, it is most commonly referred to as ADH (alcohol dehydrogenase). ADH is known to serve a number of functions in the healthy human body. In the retina it is called retinal reductase and plays a major role in vision (112), but ADH’s ability to convert alcohols to aldehydes is what is paramount to our discussion here. ADH is a large protein molecule and due to its unique structure it much “prefers” coupling with ethanol, which it converts to acetaldehyde that our body uses for many good purposes. It is only when ADH finds no ethanol in the blood or when the methanol concentration in the blood is 10 times greater than that for ethanol that ADH slowly and “reluctantly” turns methanol into formaldehyde(113,114,116-118,122). Only a small amount of ethanol in one’s blood prevents methanol from turning into formaldehyde (141). This is fortunate for without this inhibiting effect on formaldehyde formation humans would have become extinct eons ago.
Another bit of good fortune for the majority of those in the human race is something that was noticed during the development of breath analyzers for the detection of drunk drivers and subsequently confirmed in the scientific literature. That is, we nearly always have ethanol, circulating in our bloodstreams (64,188). The presence of ethanol is the natural outcome of digesting plant material in the gut(134,174), but the amounts of this endogenous ethanol in our blood varies greatly across individuals(64,173). No ethanol could be found in the blood of some subjects while others have high enough ethanol in their blood to be considered impaired (186). Individual differences in the presence of endogenous ethanol (and the location of tissue containing ADH) may well account for why some people die or become blind from a teaspoon of methanol(16) and some consume it, mixed with ethanol, as a preferred source of intoxication(110). I also believe that these individual differences in the presence of endogenous ethanol provides an explanation for why some people develop autoimmune disease and others do not, no matter what they consume or smoke.
Interestingly the location of ADH in our bodily tissue seems to vary with our genetic makeup(187). ADH might, for reasons not fully understood, be found in the liver, gut, brain, eye, skin and sinew. These hereditary differences are most likely responsible for the varied manifestations of autoimmunity. Higher enzyme representation in the brain might predispose the individual to develop MS while its presence in the skin would be required for the evolution of lupus.
Autoimmunity: Teaching our Body to Produce Antibodies against our own tissue.
During the evolution of vaccines, not long after the pioneering work of Jennings and Pasture, the pharmaceutical industry noticed and took good advantage of the “trick” of toxoid production(75,114,179). A toxoid is a bacterial or viral protein that has been treated in the laboratory with a low concentration of formaldehyde (26). The concentration is just enough to attract the attention of the macrophage but not enough to completely change the protein’s structure. The toxoid (vaccine) is injected into humans who then produce antibodies and thus develop immunity to the original, offending organism. It is interesting to note that injection of the original protein without formaldehyde treatment often causes little or no antibody production and therefore little immunity to that bacterium or virus.
As discussed in my previous article, once methanol is changed into formaldehyde and then, by water, to formal hydrate (4,27,114), all hell breaks lose.
Unbeknownst to most researchers, formal hydrate is extremely acidic(114) along with being a powerful esterifying agent (122). These two characteristics make it irresistibly attractive to our bodyÂ’s protein molecules, especially to those found in the insulation of the human brain(18,53). Opposites attract and the basic protein (MBP) of myelin quickly falls prey to acidic formal hydrate.
Macrophages are large white, amoeba like blood cells for which the major purpose in our body is to destroy attacking life forms and consume foreign and broken protein from our bodies. For reasons yet unknown, evolution has equipped macrophages with chemical receptors to detect and destroy specifically and with great vigor protein treated with formaldehyde (23,24,25). Macrophages can signal the immune system to produce antibodies to the proteins that they consume. This is a dark side to the good work of the macrophage. What happens when the protein in our brain comes in contact with formaldehyde from diet soda?
An Increase in MS
There is no denying…there has been an epidemic of autoimmune disease throughout the world over the last 30 years (79,79a-j,80,80a-c,81,81a,82). Multiple sclerosis, once almost unknown in Japan( 44,85,168), has now risen to menace a large portion of the population(81,81a). The lower latitudes and warmer climates once “mysteriously” protected from the full brunt of this tragically debilitating disease (83,85,168) have seen incidence and prevalence of MS climb to as much as four times what they were in the days before summer drinks were sweetened with Aspartame (79,79b,79d,79f,g,h,79j,80,80a-c). The United States which has long had a relatively high MS incidence has seen at least a 50% increase (77). Medical journals in Australia (82) and New Zealand (90) both report unexplainable increases in their inordinately high(168) “infection” rates.
Where Does Methanol Come from Aside from Aspartame?
Cigarette Smoking
After 150 years of study of MS only cigarette smoking is universally accepted as a causative agent(67-70,70a-d,71). Smoking has also been causally linked to the progression of MS, transforming a relapsing-remitting clinical course into a much more serious secondary progressive course (69). Tobacco leaves contain large amounts of pectin; and although most scientists are unaware of this, tobacco leaves are left in barns to ferment for weeks (61,62,66). This fermentation releases much of the available methanol from the pectin into the moisture content of the tobacco before it is sold to be made into cigarettes (65). Consequently, methanol is one of the most abundant toxic compounds found in cigarette smoke (63). Methanol is found in human breath following smoking (64) indicating a presence in the blood. A large case-controlled study, mostly of prevalent disease, has shown that systemic lupus erythematosus (SLE) is also positively associated with cigarette smoking and inversely associated with alcohol consumption(73).
Food Processing
Although acknowledging the role played by smoking, I believe that food processing and preserving is what first dramatically increased methanol consumption. At some point in our genetic history a mutation occurred that disrupted the ability of liver catalase enzyme’s to quickly and safely clean methanol from our blood (52). For several million years after this mutation there was no downside to the mutation, no autoimmunity. We ate fresh food, and what very little methanol is in fresh fruits and vegetables is countered by their own ethanol content (1,28,29)and their ubiquitous gift for slow, steady ethanol production in the gut(64,134,188). However, when the fruits and vegetables and their naturally occurring pectin is placed in a sealed container (as in canning) that is then sterilized, heated or even just stored at room temperature for months, the normally unavailable, chemically bound methanol is released from the pectin (1,28,29,34). The methanol slowly builds up, trapped in the container, to hundreds of times more than when fresh(28,29). Very simply it is “canned” fruits and vegetables that were (before aspartame) the major source of free methanol in the human diet.
The History of MS Recapitulates the History of the Canning Industry
Nicolas Appert invented canning in the 1790s, and the first canning factory was fully operational in England by 1813 (46). Due to the expense, early canning was undertaken primarily with meats which have no pectin content and therefore would not have caused methanol accumulation. However, canning of fruits and vegetables followed. Over time canning became more prevalent and less expensive(46), and the consumption of canned food skyrocketed as did the incidence of multiple sclerosis. As the canning industry flourished so did the practice of incorporating into recipes the “natural”, methanol-laden juices from canned fruits and vegetables rather than throwing them away(74).
The first documented case of multiple sclerosis was reported by Jean-Martin Charcot in a lecture in 1868(45), although it is thought that the “first identifiable instance of MS” was that of Augustus d”Este whose symptoms started between 1822 and 1843(45). During the 19th century MS was recognized as a disease but considered “quite rare” with Charcot reporting fewer than 40 cases during his long career(45). Increasing numbers of cases were reported in the late 19th century(45). Although co-occurrence is not proof of causality, similarities in initial appearance and in rate of increasing incidence are consistent with a close linkage between MS and consumption of canned fruits and vegetables.
Explaining the Unexplainable
MS a Disease of the Colder Countries
The differential prevalence of MS across different geographical regions also supports this linkage. The “latitude gradient theory” of MS is a way to explain the occurrence of higher MS prevalence in colder regions of the world (168). The tropics have until recently been blessed with very low incidence of MS (83,85,168). These warmer climes are, of course, regions in which the on-going supply of fresh fruits and vegetables has obviated the need for more expensive, canned produce, hence minimizing daily methanol consumption. The last 30 years has seen an increase in aspartame consumption in these areas and with it a significant attenuation of this gradient (91b,95)
An exception to the generalization regarding temperate regions would be expected in areas with established canning industries that are able to offer products so economically as to make the canned product a tempting alternative even in the summer months. For many years both Australia and New Zealand have had such a canning infrastructure and these countries are significant exceptions to the latitude gradient theory. Both have extremely high MS prevalence and incidence numbers (168).
Another exception (albeit in the opposite direction) is Japan which is in the colder latitudes but which has had little MS incidence through most of its recorded history(85,168). Note, however, that the Japanese cultural habit of eating everything in its season did not foster the production or importation of much canned plant material. Although far from tropical, until recently Japan has had one of the lowest rates of methanol consumption per person in the world. This rate has increased with the growing popularity of diet beverages (81,81a). The worlds largest manufacturer of Aspartame is a Japanese company.
Seasonally speaking, in the northern latitudes, before Aspartame, patients with relapsing-remitting MS could expect relapses to be experienced in the winter or Spring (72a) during periods of peak methanol consumption. With increased consumption of diet beverages, Japan and the warmer countries are now reporting their worst relapse period to be the summer (72,72a-b). The difference between warm and cool regions in remission-relapse cycles appears to parallel periods during which toxic canned vegetables and toxic thirst quenchers are most frequently consumed.
Epidemics of MS
There have also been bizarre epidemics or clusters of MS on the Faroe Islands, Orkney and Shetland Islands, and Iceland (84). All of these have been studied in great detail and all involve the influx of massive numbers of British or Allied troops (84,168). One researcher concluded that those individuals most affected were those who had been in direct contact with these troops(168). Another article goes so far as to accuse MS of being a “sexually transmitted infection”(184). An alternative explanation is that these islands had a very low incidence of MS to begin with due the lack of an established canning industry. Troops brought with them items such as canned foods, fruit preserves, marmalades and rations along with the ubiquitous cigarette, all of which would be very desirable to the island people, especially during war time. Methanol consumption was overlooked as a factor in all these studies.
The Scandinavian countries and portions of the Slavic nations have some of the highest incidence of MS of any populations in the world (95a,168). In these countries consumption of canned and home-canned fruits and vegetables is high, as is consumption of smoked-food products and traditional liquors made from rotted culled fruit. Some of these liquors have high enough methanol content to exclude them from international commerce. The alternate name for methanol is “wood alcohol” due to its original source as a condensate product made from wood smoke. Smoked meats and fish are the exception to the rule that animal products do not contain methanol.
The White ManÂ’s Burden
MS was once considered to be a “rich man’s disease” in that its prevalence was positively correlated with the trappings of civilization including modern sanitation practices (85). It now appears that consumption of canned produce provides a better explanation for the relative dearth of MS in many economically depressed regions. To this day the very poorest people of the world are free from autoimmune diseases such as MS (168), lack proper sanitation, and cannot afford canned fruits and vegetables or diet soda.
Identical Symptoms of MS, Methanol Poisoning and Aspartame Toxicity
The symptoms of multiple sclerosis (44,83,85,169), chronic and acute methanol poisoning (13,144,189), and Aspartame toxicity (54,58,93,181), are in all ways identical. There is nothing that happens to the human body from the toxic effect of methanol that has not been expressed during the course of MS…nothing (143,144). This generalization extends even to the remarkable opthomological conditions common to both: transitory optic neuritis and retrolaminar demyelinating optic neuropathy with scotoma of the central visual field (which occasionally manifests as unilateral temporary blindness (85,138,163). In fact, these opthomological symptoms have been thought of for years in their respective literatures to be “tell tale” indications for the differential diagnosis for each of these maladies independently(85,138,148,163,169). The common symptoms of headache(13,83,181,189), nervousness(13,83,181), depression (58,83,189,181), memory loss (18,147,85,169,181), tingling sensations (13,85,168,138,169), pain in the extremities (13,85,169), optic neuritis (85,138,148,163,169), bright lights in the visual field (139,83),seizures (21,83,160) inability to urinate or to keep from urinating (139,146,167) are all shared by each of these conditions and shared yet again by complaints from aspartame poisoning (54,58,93,181). I take these strikingly similar symptom patterns as evidence that these disorders act on identical components of the central nervous system and in the same way.
The “Miracle” that MS shares with Methanol poisoning
In the early stages of MS, or when a non-lethal dose of methanol has been administered, complete recovery is a possibility. The only two afflictions for which such dramatic “remissions” are reported from identical neuromuscular and opthomological damage, even “blindness” is relapsing-remitting multiple sclerosis (85) and methyl alcohol poisoning (138,163). The pathology of the two maladies is in may ways identical, particularly when it comes to destruction of the myelin sheath with no harm to the axon itself (18,148,176)
Sex Ratios for MS and Aspartame Reactions
Women bear the brunt of multiple sclerosis (91a-c) and lupus (SLE)(73) with fully three-fold representations in infliction numbers over men for both diseases. This is exactly the proportion represented by adverse reactors to Aspartame reported by the US Center for Disease Control in their study of 1984(58). The Center found three women to every man whose Aspartame consumption complaints were serious enough to warrant investigation (93). Although the female/male ratio for those stricken with MS has always been high recent estimates place it at over 3 to 1(91,91a,91c). What might account for the difference across sexes in incidence? A study published in the New England Journal of Medicine (94) reports biopsies of the gastric lining of men and women. A result was that the concentration of ADH in the gastric lining of men was much higher than for woman. Men have the advantage of removing methanol from the bloodstream four times faster on an equal-body-size basis than women. Thus, for men, methanol is more likely to be removed from the blood before it reaches the brain. The brain is spared but the methanol removed would still be metabolized to formaldehyde in the gut where it would reap its havoc on a more forgiving organ. This may help explain why men have more gastrointestinal complaints from both methanol and Aspartame consumption (93,99). On the other hand, womenÂ’s complaints from both more frequently involve serious neurological complications.
MS Cures and treatments
There are no known cures for MS and after reading about all of the many, many treatments, I conclude that the only one that shows statistically valid improvement in double-blind studies, albeit for a relatively short period of time, is plasmapheresis (186). Plasmapheresis involves removing the liquid portion (plasma) of a patientÂ’s blood, then returning the red and white blood cells to the patient without the plasma. Although not done for this reason, the process would be expected to remove much of the methanol from the bloodstream reducing its concentration substantially in the tissues. Transfusions (43) seem also to have similar effect. Viewing methanol toxicity as the ethnologic cause of MS seems to answer all of the nagging question and unexplained anomalies that have stalled the cure for this increasingly persistent disease.
Conclusion
Consumption of aspartame always results in methanol consumption (14,48,51). Methanol will always convert to formaldehyde where it finds an idle ADH (30). When this happens in the brain any protein changed by the formaldehyde will be destroyed by white blood cells (20,23,24,25). The protein most likely destroyed would be myelin basic protein MBP found in the axons. Over a long enough period of time, even without concomitant antibody production, there are those who would call this MS(44). This ends my case for considering methanol to be the cause for multiple sclerosis. Call all this hypothesis and circumstantial evidence if you like. The best experiment to confirm it would never have been allowed by any human subjects committee even though it has been going on for 27 years; and as far as I am concerned it is time to call the experiment complete and to count the bodies. Woodrow C. Monte Ph.D. Professor of Food Science (retired) Page, Arizona Note 1: It has been over 25 years since I heard my first unsolicited plea for help from an Aspartame consumer who had linked consumption of the product to her suffering. My first thought after an hourÂ’s listening was that this courageous young woman would soon be diagnosed with Multiple Sclerosis. It is in her honor that I seek to explain the compelling link between Aspartame, methanol and autoimmunity. Note 2: A fully referenced version of this article will be available at TheTruthAboutStuff.com.
Reference List
1. Monte WC. 1994. Aspartame; Methanol and the Public Health. Journal of Applied Nutrition. 36(1):42
2. Monte WC, Glanzman D. and Johnston CS. 1990. Methanol as a Model Etiologic Agent in Multiple Sclerosis. FASEB 74th annual meeting Feb 26;4(3):Abstract
3. Personal Comunication,2006. Bill Richardson, 1/1/2006
4. Kallen RG, Jencks WP. 1966. Equilibria for the Reaction of Amines with Formaldehyde and Protons in Aqueous Solution. J Biol Chem 241 (24): 5864
5. Henzi, H. 1980. The Methanol Hypothesis A New Concept of Multiple Sclerosis: (M Sr N), Juris Druck, Zurich (1980)
6. Schwyzer, RU. Henzi, H. 1983. Multiple Sclerosis: Plaques Caused by 2-Step Demyelination? Medical Hypothesis. 12:129
7. Trocho C., Pardo R, Fafecas I, Virgili J, Remesar X, Fernandez-Lopez, J A. Formaldehyde derived from dietary aspartame binds to tissue components in vivo. Life Sci 1988: 63: 337
8. Henzi, H. 1984. Chronic Methanol Poisoning with the Clinical and Pathologic-Anatomical Features of Multiple Sclerosis Medical Hypothesis. 13:63
9. Schwyzer, RU. Henzi, H. 1988. Reflections on the Pathogenesis of Optic (Retrobulbar) Neuritis in Multiple Sclerosis. Medical Hypothesis. 27:167
10. Schwyzer, RU. Henzi, H. 1992. Multiple Sclerosis: Prevention of Serious Illness – Vision of a Desired Future for Newly Ascertained Patients. Medical Hypothesis. 37:115
11. Rousseau M-C, Straif K. Siemiatycki J. 2005, IARC Carcinogen Update. Environmental Health Perspectives 113, (9) A580
12. Apol AG. 1981. Health Hazard Evaluation Report. PB82-19464 8. NIOSH U. S .Dept. of Health and Human Services HETA 81-177, 178,988 University of Washington Seattle, Washington
13. Center for Disease Control 1976. Occupational Exposure to Methyl Alcohol. U.S. Department of Health, Education, and Welfare HEW.NIOSH Pub No .(76-148)
14. Anonymous1984. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and Development. Petition submitted to the United States Food and Drug Administration - FAP 2A3661
15. Eisenberg AA. 1917. Visceral Changes in Wood Alcohol Poisoning by Inhalation. American Journal of Public Health. 7:765
16. Bennett IL, Cary FH, Michell GL. and Cooper MN. 1953. Acute Methyl Alcohol Poisoning; A Review Based on Experience in an Outbreak of 323 Cases. Medicine 32:431
17. Wimer WW, Russell JA, and Kaplan HL. 1983. Alcohols Toxicology. Alcohols Toxicology, Noyes Data Corporation. 8
18. Gaul HP, Wallace CJ, Auer RN, et al. 1995. MR findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783
19. Francot P and Geoffroy P. 1956. Le Methanol dans les jus de fruits, les boissons, fermentees, les alcools et spiritueux. Revue Des Fermentations Et Des Industries Alimentaires. 11:279
20. Davoli F. Cappellini L. Airoldi L. Fanelli R. 1986. Serum methanol concentrations in rats and in men after a single dose of aspartame. Food Chem Toxicol. 24(3):187
21. Schneck SA. 1979. Methyl alcohol. Handbook of Clinical Neurophysiology. 36:351
22. Personal Communication
23. Horiuchi S, Takata K, and Morino Y. 1985. Scavenger Receptor for Aldehyde-modified Proteins. The Journal of Biological Chemistry. 261(11):4962
24. Horiuchi S, Takata K, and Morino Y. 1985. Purification of a Receptor for Formaldehyde-treated Serum Albumin from Rat Liver. The Journal of Biological Chemistry. 260(1):482
25. Horiuchi S, Takata K, and Morino Y. 1985. Characterization of a Membrane-associated Receptor from Rat Sinusoidal Liver Cells That Binds Formaldehyde-treated Serum Albumin. The Journal of Biological Chemistry. 260(1):475
26. Metz, B., W. Jiskoot, W.E. Hennink, D.J.A. Crommelin, and G.F.A. Kersten, Physicochemical and immunochemical techniques predict the quality of diphtheria toxoid vaccines. Vaccine, 2003. 22: 156-167
27. Streitwieser A and Heathcock CH. 1985. Introduction to Organic Chemistry. Macmillan Publishing Co. 3rd Ed.:357
28. Kirchner JG and Miller JM. 1967. Volatile Water-Soluble and Oil Constituents of Valencia Orange Juice. Agricultural and Food Chemistry. 5(4):283
29. Lund ED, Kirkland CL, and Shaw PE. 1981. Methanol, Ethanol, and Acetaldehyde Contents of Citrus Products. Agricultural and Food Chemistry. 29:361
30. Koivusalo M. 1956. Studies on the Metabolism of Methanol and Formaldehyde in the Animal Organism. Acta Physiologica Scandinavica. 39.:1
31. Buys CHCM, De Jong ASH, Bouma JMW, and Gruber M. 1975. Rapid Uptake by Liver Sinusoidal Cells of Serum Albumin Modified with Retention of its Compact Conformation. Biochimica et Biophysica Acta. 392:95
32. Buys CHCM, Elferink GL, Bouma JMW, Gruber M, and Nieuwenhuis P. 1973. Proteolysis of Formaldehyde-treated Albumin in Kupffer Cells and Its Inhibition by Suramin. Journal of the Reticuloendothelial Society. 14:209
33. Gruner O and Bilzer N. 1983. Methanol content of fruit-juices. Its significance in congener analysis. Blutalkohol. 20:241
34. Casey JC, Self R, and Swain T. 1963. Origin of Methanol and Dimethyl Sulphide from Cooked Foods. Nature. 200:885
35. Braverman JBS and Lifshitz A. 1957. Pectin Hydrolysis in Certain Fruits during Alcoholic Fermentation. Food Technology. July:356
36. Campbell LA and Palmer GH. 1994. Pectin in Topics in Dietary Fiber Research. Pectin in Topics in Dietary Fiber Research, Spiller GA and Amen RJ (eds.).Plenum Press, New York, 105
37. Fink WH. 1994. The ocular pathology of methyl-alcohol poisoning. Amer J Ophthal. 26:694,802
38. Millman RB. 1982. Alcohol; The Friendly Foe. In Science Year, The World Book Science Annual. 112
39. Gordon G. 1987. UPI Investigative Report NutraSweet Questions Swirl (How Sweet It Isn't). Seattle Times Oct.:
40. Tephly TR: 1999. Comments on the purported generation of formaldehyde from the sweetener aspartame. Life Sci 65: 157-160. [ letter, not peer-reviewed]
41. Lutton JD. Winston R. Rodman TC. 2004. Multiple Sclerosis: Etiological Mechanisms and Future Directions. Experimental Biology and Medicine 229:12-20
42. Eisenberg AA. 1917. Visceral Changes in Wood Alcohol Poisoning by Inhalation. American Journal of Public Health. 7:765
43. Alexander L, Berkeley AW, and Alexander AM. 1961. Multiple Sclerosis Prognosis and Treatment. Multiple Sclerosis Prognosis and Treatment. Charles C Thomas Publisher USA
44. Hallpike JF, Adams CWM, and Tourtellotte WW. 1983. Multiple Sclerosis. Pathology, diagnosis and management, Williams & Wilkins, Baltimore
45. History of MS, 2007 Multiple Sclerosis Trust, http://www.mstrust.org.uk/information/a2z/history.jsp
46. The History of Food Canning. http://www.westlerfoods.com/pdf/canning_process.pdf
47. Scientific Abuse in Methanol / Formaldehyde Research related to Aspartame http://www.holisticmed.com/aspartame/abuse/methanol.html
48. Anonymous1994. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and Development. Petition submitted to the United States Food and Drug Administration - FAP 2A3661
49. Methanol Danger Sign, T&B Westline
50. Soffritti M. Belpoggi F. Esposti DD. Lambertini L. Tibaldi E. and Rigano A. 2006,Results of Long-Term Carcinogenicity Bioassay on Sprague-Dawley Rats Exposed to Aspartame Administered in Feed. Ann. N.Y. Acad. Sci. 1076: 559
51. Soffritti M. Belpoggi F. Cevolani D. Guarino M. Padovani M. and Maltoni C. 2002,Results of Long-Term Results of Long-Term Experimental Studies on the Carcinogenicity of Methyl Alcohol and Ethyl Alcohol in Rats N.Y. Acad. Sci. 982: 46
52. Roe O. 1982. Species Differences in Methanol Poisoning. I. Minimal Lethal Doses, Symptoms, and Toxic Sequelae of Methanol Poisoning in Humans and Experimental Apter 18,376,390. CRC Critical Reviews in Toxicology. 275
53. Rao KR, Aurora AL, Muthaiyan S, and Ramakrishnan S. 1977. Methanol toxicity - an experimental study. Bull. Jawaharlal Inst. Post-Grad.Med.Educ.Res. 2:1
54. Walton, R.G., R. Hudak, and R.J. Green-Waite. 1993. Adverse Reactions to Aspartame: Double-Blind Challenge in Patients from a Vulnerable Population. Biological Psychiatry 34:13
55. Smith EN and Taylor RT. 1982. Acute Toxicity of Methanol in the Folate-Deficient Acatalasemic Mouse. Toxicology 25:271
56. Thomas P. 2005 Aspartame: The Shocking Story of the WorldÂ’s Bestselling Sweetener. The Ecologist Sept. 36
57. Department of Health and Human Services U.S. FDA. 1979 Decision of the Public Board of Inquiry (Docket No. 75F-0355). 44 Fed. Reg. 31716
58. Center for Disease Control 1984. Evaluation of Consumer Complaints Related to Aspartame Use. Morbidity and Mortality Weekly Report. 33:605
59. Center for Disease Control 1976. Occupational Exposure to Methyl Alcohol. U.S. Department of Health, Education, and Welfare HEW.NIOSH Pub No .(76-148)
60. Office of Hon Pete Hodgson, NZ Minister of Health. 2007, Personal Communication
61. Frankenburg WG. 1950. Chemical Changes in the Harvested Tobacco Leaf. Part II. Chemical and Enzymic Conversions during Fermentation and Aging. Advances in Enzymology. 10:351
62. Neuberg C. Kobel M. 1939. Uber die encymatische Abspaltung von Methylalkohol aus Pektin durch ein Ferment dis Tabaks. Zeitschrift fĂĽr Lebensmitteluntersuchung und -Forschung A 77:3 272
63. Newsome JR, Normal V, and Keith CH. 1965. Vapor Phase Analysis of Cigarette Smoke. Tobacco Science 9:102
64. Larsson BT. 1965. Gas Chromatography of Organic Volatiles in Human Breath and Saliva. Acta Chemica Scandinavica. 19:159
65. Fellenberg T von. 1918. Uber den Nachweis und die Bestimmung des Methylalkohols, sein Vorkommen in den verschiedenen Nahrungsmitteln und das Verhalten der methylalkoholhaltland. Biochem Z. 85:45
66. Kertesz ZI. 1951. The Pectic Substances. The Pectic Substances. New York; Interscience Publishers Inc.
67. Hernan MA. Olek MJ. Ascherio A. 2001 Cigarette Smoking and Incidence of Multiple Sclerosis. American Journal of Epidemiology 154:69-74
68. Miguel AH. Jick SS. Logroscino G. Olek MJ. Ascherio A. and Jick H. Cigarette smoking and the progression of multiple sclerosis. Brain 2005 128(6):1461-1465
69. Barclay L. Lie D. Smoking May Transform Relapsing-Remitting MS Into Secondary Progressive MS. Brain. Posted online March 9, 2005. www.medscape.com/viewarticle/503872?rss
70. Hernán MA, Jick SS, Logroscino G, Olek MJ, Ascherio A, Jick H. 2005 Cigarette smoking and the progression of multiple sclerosis. Brain. 128(Pt 6):1461-5. Epub 2005 Mar 9
70a. Brey RL. 2003 Cigarette smoking and MS: Yet another reason to quit. Neurology. Oct 28;61(8):E11-2
70b. Costenbader KH, Karlson EW. Cigarette smoking and autoimmune disease: what can we learn from epidemiology? Lupus. 2006;15(11):737-45
70c. Riise T, Nortvedt MW, Ascherio A. Smoking is a risk factor for multiple sclerosis. Neurology. 2003 Oct 28;61(8):1122-4
70d. Hernán MA. Olek MJ. Ascherio A. 2001 Cigarette smoking and Incidence of Multiple Sclerosis. American Journal of Epidemiology. 154(1):69-74
71. Nortvedt MW. Riise T. Maeland JG. 2005 Multiple sclerosis and lifestyle factors: The Hordaland Health Study. Neurol Sci 26:334-339
72. Bamford RB. Sibley WA. And Thies C. 1983 Seasonal variation of multiple sclerosis exacerbations in Arizona. Neurology 33;697-701
72a. Ogawa G. Mochizuki H. Kanzaki M. Kaida K. Motoyoshi K. Kamakura K. 2003 Seasonal variation of multiple sclerosis exacerbations in Japan. Neurol Sci 24;417-419
72b. Abella-Corral J. Prieto JM. Dapena-Bolaño D. Iglesias-GĂłmez S. Noya-GarcĂa M. Lema M. 2005 (Seasonal variations in the outbreaks in patients with multiple sclerosis) Rev Neurol 40(7):394-396
73. Hardy CJ. Palmer BP. Muir KR. Sutton AJ. Powell RJ. 1998 Smoking history, alcohol consumption, and systemic lupus erythematosus: a case-control study Ann Rheum Dis 57:451-455
74. Landtblom A-M. Flodin U. Sodeifeldt B. Wolfson C. Axelson O. 1996, Organic Solvents and Multiple Sclerosis: A Synthesis of the Current Evidence Epidemiology Vol.7 # 4 429-433
75. Grabenstein JD. 2006 Excipient content of U.S. Vaccines ImmunoFacts: Vaccines & Immunologic Drugs. St. Louis, MO: Wolters Kluwer Health Inc.
76. Weiner HL. Dau PC. Khatri BO. Petajan JH. Birnbaum G. McQuillen MP. Fosburg MT. Feldstein M. Orav EJ. 1989 Double-blind study of true vs. sham plasma exchange in patients treated with immunosuppression for acute attacks of multiple sclerosis. Neurology. 39(9):1143-9
77. Hirtz D. Thurman DJ. Gwinn-Hardy K. Mohamed M. Chaudhuri AR. Zalutsky R. 2007 How common are the "common" neurologic disorders? . Neurology. 68:326-337
78. Monte WC. 2007 Is your Diet Sweetener Killing You? Fitness Life 33: 30-33
79. Corona T. Roman GC. 2005 Multiple Sclerosis in Latin America. Neuroepidemiology 26: 1-3
79a. Celius EG. Vandvik B. 2001 Multiple sclerosis in Oslo, Norway: prevalence on 1 January 1995 and incidence over a 25-year period. European Journal of Neurology 8:(5) 463
79b. Barnett MH. Williams DB. Day S Macaskill P. McLeod JG. 2003 Progressive increase in incidence and prevalence of multiple sclerosis in Newcastle, Australia: a 35-year study. J Neurol Sci. 15;213(1-2):1-6.
79c. Sumelahti ML, Tienari PJ, Wikström J, Palo J, Hakama M. 2001 Increasing prevalence of multiple sclerosis in Finland Acta Neurol Scand. 103(3):153-8
79d. Pugliatti M. Sotgiu S. Solinas G. Castiglia P. Pirastru MI. Murgia B. Mannu L. Sanna G. Rosati G. 2001 Multiple sclerosis epidemiology in Sardinia: evidence for a true increasing risk. Acta Neurol Scand. 103(1):20-6
79e. Sundström P. Nyström L. Forsgren L. 2003 Incidence (1988-97) and prevalence (1997) of multiple sclerosis in Västerbotten County in northern Sweden. J Neurol Neurosurg Psychiatry. 74(1):29-32
79f. Pugliatti M. Riise T. Sotgiu MA. Sotgiu S. Satta WM. Mannu L. Sanna G. Rosati G. 2005 Increasing incidence of multiple sclerosis in the province of Sassari, northern Sardinia. Neuroepidemiology 25(3):129-34. Epub 2005 Jun 29.
79g. Pozzilli C. Romano S. Cannoni S. 2002 Epidemiology and current treatment of multiple sclerosis in Europe today. J Rehabil Res Dev. 39(2):175-85
79h. Pugliatti M. Sotgiu S. Rosati G. 2002 The worldwide prevalence of multiple sclerosis. Clin Neurol Neurosurg. 104(3):182-91.
79i. Gallagher L, Lea R. 2005 The epidemiology of multiple sclerosis in New Zealand. N Z Med J. 118(1212):U1396.
79j. Ranzato F, Perini P, Tzintzeva E, Tiberio M, et. al. 2003 Increasing frequency of multiple sclerosis in Padova, Italy: a 30 year epidemiological survey. Mult Scler. 9(4):387-92.
80. Grimaldi LM. Palmeri B. Salemi G. Giglia G. D'Amelio M. Grimaldi R. Vitello G. Ragonese P. Savettieri G. 2007 High prevalence and fast rising incidence of multiple sclerosis in Caltanissetta, Sicily, southern Italy. Neuroepidemiology. 28(1):28-32. Epub 2006 Dec 8.
80a. Barnett MH. Williams DB. Day S Macaskill P. McLeod JG. 2003 Progressive increase in incidence and prevalence of multiple sclerosis in Newcastle, Australia: a 35-year study. J Neurol Sci. 15;213(1-2):1-6.
80b. Granieri E. Casetta I. Govoni V. Tola MR. Marchi D. Murgia SB. Ticca A. Pugliatti M. Murgia B. Rosati G. 2000 The increasing incidence and prevalence of MS in a Sardinian province. Neurology 26;55(6):842-8
80c. Grimaldi LM. Salemi G. Grimaldi G. Rizzo A. Marziolo R. Lo Presti C. Maimone D. Savettieri G. 2001 High incidence and increasing prevalence of MS in Enna (Sicily), southern Italy. Neurology 57(10):1891-3
81. Kira J. 2006 Epidemiology of multiple sclerosis in Japanese: with special reference to opticopsinal multiple sclerosis. Rinsho Shinkeigaku. 46(11):859-62
81a. Tanaka K, Kujuro Y, Suzuki S, Tanahashi N, Hamada J, Nogawa S, Suzuki N. Clinical and laboratory features of in-patients with multiple sclerosis in a University Hospital in Tokyo from 1988-2002. Intern Med. 2005 Jun;44(6):560-6
82. Access Economics, 2005 Acting Positively: Strategic Implications of the Economic costs of Multiple Sclerosis in Australia www.ms.org.au/msinformation/articles/MSFINALREPORTWINTER2005.pdf
83. Lazoff M. 2005 Multiple Sclerosis Symptoms. eMedicin WebMD www.emedicine.com/emerg/topic321.htm#section%7Eauthor_information
84. Waksman B. 1985 Mechanisms in multiple sclerosis. Nature 318: 104
85. Leibowitz U and Alter M. 1973. Multiple Sclerosis: Clues to its cause. North-Holland Publishing Co.
86. Kieseier B. Hemmer B. Hartung HP. 2005 Multiple Sclerosis –novel insights and new therapeutic strategies. Current Opinion in Neurology 18:211- 220
87. Ibrahim SM. Gold R. 2005 Genomics, promeomics, metabolomics: what is in a word for multiple sclerosis. Current Opinion in Neurology 18:231 – 235
88. Wikipedia, the free encyclopedia. 2007 Glial cell. http://en.wikipedia.org/wiki/Glial_cell
89. National Toxicology Program, U.S. Department of Health and Human Services. 2001 NTP-CERHR Expert Panel Report on Reproductive and Developmental Toxicity of Methanol, Draft 7/17/01
90. Gallegher L. Lea R. 2005 The epidemiology of multiple sclerosis in New Zealand. The New Zealand Medical Journal 118: 1212
91. Boyles S. 2007 MS Increasingly a WomanÂ’s Disease. MedicineNet.com www.medicinenet.com/script/main/art.asp?articlekey=80722
91a. Cutter G. et. al. 2007 Changes in the Sex Ratio over Time in Multiple Sclerosis. 59th Annual Meeting of the American Academy of Neurology, Boston April 28 – May 5, 2007
91b. Hernán MA. Olek MJ. Ascherio A. 1999 Geographic variation of MS incidence in two prospective studies of US women. Neurology 53(8):1711-8
91c. Noonan CW, Kathman SJ, White MC. 2002 Prevalence estimates for MS in the United States and evidence of an increasing trend for women. Neurology 58(1):136-8
92. Health Effects Institute 1999 Reproductive and offspring Developmental Effects Following Maternal Inhalation Exposure to Methanol in Nonhuman Primates. Research Report Number 89
93. Anonymous1984. Evaluation of Consumer Complaints Related to Aspartame Use. Morbidity and Mortality Weekly Report. 33:605
94. Frezza M, di Padova C, Pozzato G, Terpin M, Baraona E, Lieber CS. 1990 High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. N Engl J Med. 322(2):95-9
95. Pugliatti M, Sotgiu S, Solinas G, Castiglia P, Rosati G. 2001 Multiple sclerosis prevalence among Sardinians : further evidence against the latitude gradient theory Neurol Sci. 2001 Apr;22(2):163-5
95a. Rosati G. 2001 The prevalence of multiple sclerosis in the world: an update Neurol Sci 22:117-139
96. Mahalik MP and Gautieri RF. 1984. Reflex Responsiveness of CF-1 Mouse Neonates Following Maternal Aspartame Exposure. Res Commun in Psych. 9:385
97. National Toxicology Program, U.S. Department of Health and Human Services. 2002 NTP-CERHR Expert Panel Report on Reproductive and Developmental Toxicity of Methanol NTP-CERHR-MeOH-02
98. FightingAutism.org Number of Cases http://www.fightingautism.org/idea/autism.php?
99. Gettler AO. St.George AV. 1918. Wood Alcohol Poisoning. Journal of the American Medical Association. 70:145.
100. Sturtevant FM. 1985. Use of Aspartame in Pregnancy. Int J Fertil. 30(1):85
101. Anonymous1982. Therapeutic claims in multiple sclerosis. National Multiple Sclerosis Society. National Multiple Sclerosis Society. Jan.:49
102. Sturtevant FM. 1985. Does Aspartame Cause Methanol Toxicity? Fd Chem Toxic. 23(10):961
103. Infurna R. Weiss B. 1986 Neonatal Behavioral Toxicity in Rats Following Prenatal Exposure to Methanol Teratology 33:259-265
103a. Infurna R, Schubin W, and Weiss B. 1981. Developmental Toxicology of Methanol. Toxicologist 1:32
104. Bolon B, Dorman DC, Janszen D, Morgan KT, Welsch F. 1993 Phase-specific developmental toxicity in mice following maternal methanol inhalation. Fundam Appl Toxicol. 21(4):508-16
105. Dorman DC, Bolon B, Struve MF, LaPerle KM, Wong BA, Elswick B, Welsch F. 2005 Role of formate in methanol-induced exencephaly in CD-1 mice. Teratology. 52(1):30-40
106. Potts AM, Praglin J, Farkas J, Orbison L, and Chickering D. 1976. Studies on the Visual Toxicity of Methanol. VIII. Additional Observations on Methanol Poisoning in the Primate Test Object. Amer J Ophthal. 40:76
107. Kavet R and Nauss KM. 1990. The Toxicity of Inhaled Methanol Vapors. Critical Reviews in Toxicology. 21:21
108. Rabinovitch and MD IM. 1922. Biochemical Studies in a Fatal Case of Methyl Alcohol poisoning. Archives of Internal Medicine, Chicago. 29:821
109. Kane RL, Talbert W, Harlan J, Sizemore G, and Cataland S. 1968. A methanol poisoning outbreak in Kentucky. A clinical epidemiological study. Arch Environm Hlth. 17:119
110. Menne FR. 1935. Acute Methyl Alcohol Poisoning, a Report of Twenty-Two Instances with Postmortem Examinations. Archives of Pathology. 26:77
111. Bennett IL, Cary FH, Michell GL. and Cooper MN. 1953. Acute Methyl Alcohol Poisoning; A Review Based on Experience in an Outbreak of 323 Cases. Medicine 32:431
112. Kini MM and Cooper JR. 1961. Biochemistry of Methanol Poisoning-III; The Enzymic Pathway for the Conversion of Methanol to Formaldehyde. Biochemical Pharmacology. 8:207
113. Kini MM and Cooper JR. 1962. Biochemistry of Methanol Poisoning; The Effect of Methanol and its Metabolites on Retinal Metabolism. Biochemical Journal. 82:164
114. French D and Edsall JT. 1945. The Reactions of Formaldehyde with Amino Acids and Proteins. Adv.Protein Chem 2:277
115. Leaf G and Zatman LJ. 1952. A Study of the Conditions Under Which Methanol May Exert a Toxic Hazard in Industry. British Journal of Industrial Medicine. 9:19
116. Cooper JR and Kini MM. 1962. Biochemical Aspects of methanol Poisoning. Biochemical Pharmacology. 11:405
117. Cooper JR and Felig P. 1961. The Biochemistry of Methanol Poisoning. II. Metabolic Acidosis in the Monkey. Toxicol.Appl.Pharmacol. 3:202
118. Clay KL, Murphy RC, and Watkins WD. 1975. Experimental Methanol Toxicity in the Primate; Analysis of Metabolic Acidosis. Toxicol.Appl.Pharmacol. 34:49
119. McLean DR, Jacobs H, and Mielke BW. 1979. Methanol Poisoning A Clinical and Pathological Study. Annals of Neurology 8:161
120. Posner HS. 1975. Biohazards of Methanol in Proposed New Uses. J.Toxicol.Environ.Health 1:153
121. Stegink LD. Filer LJ Tephly TR. Aspartame – The Book, Marcel Dekker, Inc New York
122. von Oettingen WF. 1943. The Aliphatic Alcohols Their Toxicity and Potential Dangers in Relation to Their Chemical Constitution and Their Fate in Metabolism. Public Health Bulletin 281:1
123. Siragusa RJ, Cerda JJ, Baig MM, Burgin CW, and Robbins FL. 1988. Methanol production from the degradation of pectin by human colonic bacteria. American Journal of Clinical Nutrition. 47:848
124. Nelson BK, Brightwell WS, MacKenzie DR, Khan A, Burg JR, Weigel WW, and Goad P. 1985. Teratological Assessment of Methanol and Ethanol at High Inhalation Levels in Rats. Fundam Appl Toxicol. 5:727
125. Sollmann T. 1920. Studies of chronic intoxications on albino rats. II. Alcohol; Methyl, ethyl, "wood" and acetone. J Pharmacol Exper Therap. 16:291
126. Victor M. 1977. Some Observations on the Neurological Effects of Alcohol Intoxication and Withdrawal. Neurotoxicology Raven Press, New York 517
127. Smith SR, Smith SJM, and Buckley BM. 1981. Combined Formate and Lactate Acidosis in Methanol Poisoning. The Lancet. 1:1295
128. Fulop, M. 1982. Methanol Intoxication. The Lancet Feb.:338
129. Roe, O. 1948. The Ganglion Cells of the Retina in Cases of Methanol Poisoning in Human Beings and Experimental Animals. Acta Opthalmologica 26:169
130. Potts AM. 1984. The Aliphatic Alcohols. Handbook of Experimental Pharmacology. 69(Pharm. Eye):639
131. Martin-Amat G, McMartin KE, Hayreh SS, Hayreh MS, and Tephly TR. 1978. Methanol Poisoning Ocular Toxicity Produced by Formate. Toxicology and Applied Pharmacology. 45:201
132. Makar AB, Tephly TR, and Mannering GJ. 1968. Methanol Metabolism in the Monkey. Molecular Pharmacology. 4:471
133. Majchrowicz E. 1973. Biochemical Pharmacology of Ethanol. Biochemical Pharmacology of Ethanol. Plenum Press, New York 122
134. Majchrowicz E and Mendelson JH. 1971. Blood Methanol Concentrations During Experimentally Induced Ethanol Intoxication in Alcoholics. The Journal of Pharmacology and Experimental Therapeutics. 179:293
135. Magrinat G, Dolan JP, Biddy RL, Miller LD, and Korol B. 1973. Ethanol and Methanol Metabolites in Alcohol Withdrawal. Nature. 244:234
136. Walder AI, Redding JS, Faillace L, and Steenberg W. 1969. Rapid Detoxification of the Acute Alcoholic with Hemodialysis. Surgery. 66:201
137. Guggenheim MA, Couch JR, and Weinberg W. 1971. Motor Dysfunction as a Permanent Complication of Methanol Ingestion. Archives of Neurology. 24:550
138. Scott E, Helz MK, and McCord CP. 1933. The Histopathology of Methyl Alcohol Poisoning. American Journal of Clinical Pathology. 3:311
139. Keyvan-Larijarni H and Tannenberg AM. 1974. Methanol Intoxication; Comparison of Peritoneal Dialysis and Hemodialysis Treatment. Arch Intern Med 134:293
140. Gronning M. Albrektsen G. Kvale G. Moen B. Aarli JA. Nyland H. 1993 Organic solvents and multiple sclerosis: a case-control study. Acta Neurol Scand 88: 247-250
141. Agner K, Hook O, and von Porat B. 1949. The Treatment of Methanol Poisoning with Ethanol. With Report of Two Cases. Quarterly Journal of Studies on Alcohol. 9:515
142. Roe O. 1950. The roles of Alkaline salts and Ethyl Alcohol in the treatment of Methanol Poisoning (1164). Quart.J.Stud.Alcohol. 11:107
143. Erlanson P, Fritz H, Hagstam K-E, Liljenberg B, Tryding N, and Voigt G. 1965. Severe Methanol Intoxication. Acta Medica Scandinavica. 177(4):393
144. Browning E. 1965. Methanol Toxicology. In Toxicity and Metabolism of Industrial Solvents. Elsevier Publishing Company, New York 315-323
145. Humphries P. Pretorius E. Naud H. 2007 Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. Aug 8; 1-12
146. Isaacs R. 1920. Acute Methyl Alcohol Poisoning. J.Am.Med.Assoc.or JAMA 75:718
147. Pick L and Bielschowsky M. 1912. Ueber histologische Befunde im Auge and im Zentralnervensystem des Menschen bei akuter todlicher Vergiftung mit Methylalkohol. Klin Wschr. 49:888
148. Sharpe JA, Hostovsky M, Bilbao JM, and Rewcastle NB. 1982. Methanol optic neuropathy; A histopathological study. Neurology (Ny) 32:1093
149. Waksman BH and Reynolds WE. 1984. Multiple Sclerosis as a Disease of Immune Regulation (41798). Proceedings of the Society for Experimental Biology and Medicine 175:282
150. Pohl J. 1893. Ueber die Oxydation des Methyl Und Aethylalkohols im Thierkorper. Naunyn-Schmiedeberg's Arch exp Path Pharmak. 31:281
151. Anderson CA, Rubinstein D, Filley CM, Stears JC. 1997 MR enhancing brain lesions in methanol intoxication. J Comput Assist Tomogr. 1997 Sep-Oct;21(5):834-6
152. Fackelmann KA. 1990. Myelin on the Mend: Can antibodies reverse the ravages of multiple sclerosis?. Science News. 137:218
153. Wolfgang F. 1979. What if Multiple Sclerosis isnÂ’t an Immunological or Viral Disease? The Case for a Circulating Toxin. Neurochemical Research 4:1-14
154. Adams CWM. 1981. Histochemical Contributions to the Study of Multiple Sclerosis. Histochemistry The Widening Horizons. Edited by P.J. Stoward and J. M. Polak 163
155. Alexander L, Berkeley AW, and Alexander AM. 1961. Multiple Sclerosis Prognosis and Treatment. Multiple Sclerosis Prognosis and Treatment. Charles C Thomas Publisher USA
156. Brown MS and Goldstein JL. 1983. Lipoprotein Metabolism in the Macrophage; Implications for Cholesterol Deposition in Atherosclerosis. Annu Rev Biochem. 52:223
157. Tephly TR. 1977. Factors in Responses to the Environment. Introduction. Federation Proceedings. 36(5):1627
158. Blundell JE and Hill AJ. 1986. Paradoxical Effects of an Intense Sweetener (Aspartame) on Appetite. Lancet May:1092
159. Coulombe RA Jr. and Sharma RP. 1986. Neurobiochemical Alterations Induced by the Artificial Sweetener Aspartame (NutraSweet). Toxicology and Applied Pharmacology. 83:79
160. Walton RG (1128). 1986. Seizure and Mania After High Intake of Aspartame. Journal of the Academy of Psychosomatis Medicine, Apr.:218
161. Roak-Foltz R and I. Leveille GA.Marcel Dekker. 1984. Projected Aspartame Intake: Daily Ingestion of Aspartic Acid, Phenylalanine, and Methanol Aspartame – The Book, Marcel Dekker, Inc New York 201
162. Main, R.H. 1903. On The Toxicity of Methyl Alcohol in Extracts and Medicine. Illinois Medical Journal 153
163. Koller, C. 1905. Poisoning by Wood Alcohol: A case of Complete Blindness (Transitory) with Recovery of Vision. Medical Record 1vxiii:10
164. Medical Record 1905 Excerpts from Doctors Letters
165. Wood, C.A. 1906. Death and Blindness as a Result of Poisoning by Methyl Alcohol or Wood Alcohol and Its Various Preparations. International Clinics; A Quarterly of Clinical Lectures 16:68
166. Kritchevsky M. 1988. Multiple Sclerosis. In Wiederholt WC, Ed.Neurology for Non-Neurologists.Philadelphia, Harcourt
167. Blaivas JG. 1984. Evaluation of Urinary Bladder Symptoms in Multiple Sclerosis. The Diagnosis of Multiple Sclerosis. Ed. Poser CM.Thieme-Stratton Inc. 76
168. Kurtzke JF. 1980. Epidemiologic contributions to multiple sclerosis; An overview. Neurology. Neurology 30(7):61
169. Matthews B. 1978. Multiple sclerosis The Facts. Multiple sclerosis The Facts. Oxford University Press
170. Mawdsley C and Mayer RF. 1965. Nerve Conduction in Alcoholic Polyneuropathy. Brain 88:335
171. Benton CD and Calhoun FP. 1952. The Ocular Effects of Methyl Alcohol Poisoning. Report of a Catastrophe involving Three Hundred and Twenty Persons. Trans Amer Acad Ophthal Otolaryng. 56:875
172. Yano K, Rhoads GG, and Kagan A. 1977. Coffee, Alcohol and Risk of Coronary Heart Disease Among Japanese Men Living in Hawaii. New England Journal of Medicine. 297:405
173. Lester D. 1961. Endogenous Ethanol; A Review. Quarterly Journal of Studies on Alcohol. 22:555
174. Lester D. 1962. The Concentration of Apparent Endogenous Ethanol. Q. J. Stud. Alcohol 23:17
175. Lieber CS and DeCarli LM. 1970. Hepatic Microsomal Ethanol-Oxidizing System. In vitro characteristics and adaptive properties in vivo. The Journal of Biological Chemistry. 245:2505
176. Klatsky AL, Friedman GD, and Siegelaub AB. 1981. Alcohol and Mortality. Annals of Internal Medicine. 95:139
177. Hoque M, Monte WC, and Johnston CS. 1988. Methanol Neuropathy A Histological Study on Long-Evans Rats. FASEB J 25;2(6):A513
178. Benditt EP. 1994. The Origin of Atherosclerosis. Scientific American. 236:74
179. Metz, B. GFA Kersten GFA. Jong A. Meiring H. 2005 Identification of formaldehyde-induced modifications in proteins: reactions with diphtheria toxin http://igitur-archive.library.uu.nl/dissertations/2005-0303-105230/c7.pdf
180. Gombos K. et.al. 2007 The effect of aspartame administration on oncogene and suppressor gene expressions. In Vivo 21(1): 89-92
181. Grey DM. 1995 Summary of Adverse Reactions Attributed to Aspartame. US Department of Health and Human Services. Personal Communication
182. Humphries P. Pretorius E. and Naude H. 2007 Direct and indirect cellular effects of aspartame on the Brain. European Journal of Clinical Nutrition 2007:1-12
183. Parthasarathy NJ. Kumar RS. Manikandan S. Devi RS 2006 Methanol-Induced Oxidative Stress in Rat Lymphoid Organs. J. Occup Health 48:20-27
184. Hawkes CW. 2002 Is multiple sclerosis a sexually transmitted infection. J Neurol Neurosurg Psychiatry. 73(4):439-43.
185. Kantarci O. Wingerchuk D. 2006 Epidemiology and natural history of multiple sclerosis: new insights. Curr Opin Neurol 19:248-254
186. Dahshan A. Donovan K. 2001 Auto-Brewery Syndrome in a Child With Short Gut Syndrome: Case Report and Review of the Literature. Journal of Pediatric Gastroenterology and Nutrition 33:214–215
187. Borras E. et. al. 2000. Genetic Polymorphism of Alcohol Dehydrogenase in Europeans: The ADH2*2 Allele Decreases the Risk for Alcoholism and Is Associated With ADH3*1. HEPATOLOGY Vol. 31, No. 4
188. Erickson SP. Kulkarni AB. 1963. Methanol in Normal Human Breath. Science 141:639
189. Wood CA and Buller F. 1904. Poisoning by Wood Alcohol. J.Am.Med.Assoc.or JAMA 43:972,1058,1117,1213,1.
190. Kingsbury K. 2007. The Changing Face Of Breast Cancer. TIME Magazine October 15th, 2007:36
